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Background The altered expressions of hippocampal N-methyl-D-aspartate (NMDA) receptors induced by benzo[ɑ]pyrene (BaP) causes short-term spatial learning and memory impairment in humans and animals, but whether BaP causes alterations of NMDA receptor subunits in other brain regions and the associated neurotoxic mechanism is still essentially unknown. Objective To observe the mRNA expressions of NR1, NR2A, and NR2B of NMDA receptor subunits in different brain regions in SD rat model with subchronic exposure to BaP, and to provide a basis for in-depth study of the mechanism of BaP-induced neurotoxicity. Methods Forty male SD rats were selected and randomly divided into a control group and 1.00, 2.50, and 6.25 mg·kg−1 BaP exposure groups with 10 rats in each group. The exposure rats received intraperitoneal injection of BaP every other day for 90 d.The average latency to platform, the average total distance, and the duration spent in previous quadrant were measured by the Morris Water Maze. Real-time fluorescence quantitative PCR was used to detect the mRNA expressions of NR1, NR2A, and NR2B in hippocampus, cortex, cerebellum, and striatum of rats. Results The average latency to platform and the average total distance in the 2.50 and 6.25 mg·kg−1 BaP groups were significantly prolonged compared with the control group (P<0.05), and the duration that rats spent in previous quadrant in the 6.25 mg·kg−1 BaP group was significantly shortened (P<0.05). Compared with the control group, the mRNA expressions of NR1 and NR2B in the hippocampus in the 2.50 and 6.25 mg·kg−1 BaP groups were significantly reduced (P<0.05), and the NR2A mRNA expression in the hippocampus in the 6.25 mg·kg−1 BaP group was significantly reduced (P<0.05); the mRNA expressions of NR1 and NR2B in the cortical tissue in the 6.25 mg·kg−1 BaP group were significantly reduced (P<0.05), and the mRNA expression of NR2A in the cortical tissue in the 1.00 mg·kg−1 BaP group was reduced; the mRNA expression of NR2B in the cerebellar tissue in the 6.25 mg·kg−1 BaP group was significantly reduced (P<0.05); there were no differences in the mRNA expressions of NMDA receptor subunits in the striatum tissue (P>0.05). Conclusion Subchronic BaP exposure can cause short-term spatial learning and memory impairment in rats, which may be related to the down-regulation of mRNA expressions of NR1, NR2A, and NR2B in hippocampus, changes of mRNA expressions of NR1, NR2A, and NR2B in cortical area, and the down-regulation of NR2B mRNA expression in cerebellum.
RESUMO
<p><b>OBJECTIVE</b>In this study, we investigate the relationship between HSP70 and lung function injury. To study on the feasibility of HSP70 genes polymorphisms as biological marker of the damage of pulmonary dysfunction susceptibility.</p><p><b>METHODS</b>183 cock-oven workers were selected as exposure groups and 143 workers unexposed workers were selected as control groups. We investigated their general information with uniform questionnaire. Pulmonary dysfunction indicators were determined using portable spirometer. HSP70-1 G190C, HSP70-2 A1267G, HSP70- hom T2437C genotypes were analyzed by using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. The haplotypes were calculated using PHASE 2.0 software.</p><p><b>RESULTS</b>VC%, FVC%, MVV%, FEV(1.0%) in exposed group were lower than in non-exposure group, the difference were significantly (P < 0.05). VC%, FVC%, MVV%, FEV1.0% in exposed group with HSP70-1, HSP70-2, HSP70-hom genotypes were lower than in non-exposure group (P < 0.05); FVC% in exposed group with HSP70-hom T/C genotypes were lower than that with HSP70-hom T/T genotypes, MVV% were lower than that with HSP70-hom T/T, C/C genotypes. There's no difference in pulmonary dysfunction index of HSP70-1, HSP70-2 genotypes (P>0.05), but significant difference between the exposed group with HSP70-1, HSP70-hom genotypes; The adjust OR (95%CI) of exposed group with HSP70-1 G/C genotypes and HSP70-homT/C genotypes were 2.516 (1.012 ∼6.252) and 2.284 (1.033∼5.053). Exposed group with CGT haplotype pulmonary dysfunction were significantly higher than in non-exposure group (P < 0.05).</p><p><b>CONCLUSION</b>Coke oven exposure may increase pulmonary dysfunction injury, Coke oven workers who have the HSP70-1 G/C genotypes, HSP70-hom T/C genotypes and CGT haplotypes may increase the susceptibility of pulmonary dysfunction. There must be some relationship between HSP70-1, HSP70-hom gene polymorphisms and lung function injury of Cock-oven Workers.</p>